Experiments are directed toward establishing whether aged mice are deficient in their ability to form long-term memory and whether administration of neuropeptides can retard forgetting in both young-mature and aged mice. Although there are many claims that old rodents forget rapidly, as yet few studies have controlled for the possibility that rapid forgetting in old rodents is due to variables operating during learning (e.g., motivation, footshock sensitivity) rather than to an alteration in the physiological mechanisms subserving memory fixation. The proposed studies will attempt to determine whether in fact aged mice forget more rapidly than young mice when degree and rate of learning are controlled for. Central release of vasopressin has been implicated as being a requisite for efficient memory fixation. An impaired ability of old mice to form durable long-term memory may be due to a diminished ability to synthesize and/or secrete vasopressin. Thus, administration of vasopressin may enhance memory consolidation. Experiments are designed to examine the anterograde and retrograde effects of parentral and central vasopressin injections on forgetting in both old and young mice. Aside from determining the temporal features of vasopressin-induced memory enhancement, we plan to use local injections to determine which brain sites mediate neuropeptide-induced memory ehancement, and whether vasopressin enhances memory by stimulating protein synthesis. Additional experiments will attempt to determine whether vasopressin enhances retention by changing the content of the engram or whether it protects memory from environmental factors that lead to memory degradation.